The lessons science and pharmacology teach us about
achieving optimal health, vitality and maximal lifespan with a low net carb, high saturated fat, evolutionarily paleolithic-styled diet aligned with my ancestral heritage and how I lost 50 pounds of body fat. A sorta fairy story.

The diagram exemplifies a normal coronary artery, with a large.. wide diameter... spacious... flexible.. lumen (Courtesy: medicinenet.org). The diameter of the artery can be measured accurately down to fractions of a millimeter via angiography.

It was observed that in post-menopausal women with documented heart disease from the Estrogen Replacement and Atherosclerosis (ERA) trial, a multicenter clinical trial evaluating the effects of hormone replacement therapy on atherosclerotic progression, in the group consuming the highest-saturated dietary fat diet (12.0% Sat Fat), an enlargement in coronary diameter of 0.01 mm and a 0.1% regression in coronary artery stenosis.

Quoted to Men's Health, "In the nutrition field, it's very difficult to get something published that goes against established dogma," said Dr. Dariush Mozaffarian MD MPH, assistant professor, Harvard. "The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence." Mozaffarian says he believes it's critical that scientists remain open minded. "Our finding was surprising to us. And when there's a discovery that goes against what's established, it shouldn't be suppressed but rather disseminated and explored as much as possible."

In a year during my pharmacy student training at Stanford, I worked with Dariush on an internal med rotation for 4wks. I think I learned more about drugs and how to use them than some of my preceptors combined. His teaching approaches were usually articulate, concise and patiently provided. Gosh, can I say, I've had serendipity with many mentors in my little drug journey so far. *haa*

Dividing the saturated fat intake into quartiles, the individuals at the highest quartile (dietary saturated fat intake: 12.0%) demonstrated the least progression on angiogram of coronary diameter. In fact, this was the only group that exhibited REGRESSION.

Lipid-Lowering Drugs: The Less, The More RegressionThe researchers astutely noticed that "among the women not taking lipid-lowering medication at baseline or during follow-up, there was 0.22 mm less progression for each 5% greater energy intake from saturated fat, compared with 0.09 mm less progression for each 5% greater energy intake from saturated fat among women taking lipid-lowering medication (P = for interaction 0.008)."

Omega-6 PUFAs: Highly Associated with ProgressionAfter the Lyon-Diet Heart trial was completed and showed a dramatic reduction in all-cause mortality, cardiac death and events with simple reductions in omega-6 PUFAs and increase omega-3 from fish and ALA sources like olive oil, I think this trial hits it home again that any increase in dietary PUFAs are extremely pro-inflammatory leading to progression of coronary artery diameter reductions. The lowest quartile consumed less than 3.9% PUFA which was positively (see above) associated with less of a decline of average minimal coronary artery diameter (P for trend =0.04) compared with other quartiles. Clearly, a dietary PUFA concentration greater than 3.9% was highly statistically correlated to angiogram progression. The highest quartile that consumed 7.5% PUFA in the diet this was shown to produce the second highest amount of artery diameter constriction in this trial.

FIGURE 1 (divided, above, below). Mean (SE) change in minimal coronary artery diameter according to intake of different nutrients, with adjustments as in Table 2 (see footnote 1), except that total fat was not adjusted for carbohydrate, and carbohydrate and protein were also adjusted for polyunsaturated fat. These models estimate the effect of saturated fat replacing other fats (monounsaturated or polyunsaturated),monounsaturated fat replacing other fats (saturated or polyunsaturated), polyunsaturated fat replacing other fats (saturated or monounsaturated), total fat replacing carbohydrate, carbohydrate replacing saturated or monounsaturated fat, and protein replacingsaturated or monounsaturated fat.

When I hear an HDL cholesterol is off the charts, like triple-digit-over-100 mg/dl... you my dear have my full attention.

HDL Cholesterol: The Higher, The HOTTER

HAWT HDLs.

The goal for health optimization for HDL-cholesterol is 60 mg/dl or higher. Studies like the Four Prospective American Studies by Castelli WP et al found "A 1-mg/dl increment in HDL-C was associated with a significant coronary heart disease risk decrement of 2% in men (Framingham/FHS, CPPT, and MRFIT) and 3% in women (FHS)."

According to master cardiologist Dr. Castelli (who has successfully escaped premature family hx of CAD), if one's baseline HDLs are 30's and one increases this to 80's, this may represent a 100% reduction in relative risk for a coronary event. For girls, if one increases from HDLs 50's to 80's, then also a 100% coronary risk reduction could be relied upon.

Sounds excellent to me!

It is not difficult to raise HDLs.

This is observed all over in the evolutionary/paleo blogosphere, at Bernstein's diabetes, Protein Power Drs.Eades blog, at TYP in only those on high sat fat and/or [no or low-statin+wt-loss] and in clinical practice ALL THE TIME.

Eliminating wheat/d*mn-dirty-GRAINS/carbs, adding some vitamin D, omega-3s, Taurine, and Slo-Niacin 1-2 grams/day. Throwing away the Mazola and any packaged food items. Oh yeah, and add some fat. Individuals may continue their EVO (but not too much b/c it cranks up hepatic lipase, see HERE) but they increase eggs 2-6 daily, add some (organic nitrate-free preferably) bacon and some coconut oil.

And...reduce their statin (if even taking).

I know, s a c r i l e g e . . .

Consider the value of not over-statinating.

Over-statinating stagnates the formation of large particles. wtf. This is observed on the TYP forum frequently in over-statinators -- and easily corrected. The statin or fibrate is withheld or severely dose-reduced (TYPically, I advise 'licking the tablet' and that is a clinical term). See below medscape cases as well.

Yes, statins and fibrates LOWER HDLs ('good chol') for many individuals. Lipitor is the worse. Drugs appear to cause a 'ceiling' effect for HDLs and small dense LDL. Marginally on paper these may improve, however iatrogenically they fail to improve FURTHER beyond the ceiling.

Esp if low sat fat.

Esp additionally if you are an apo E2 carrier (you have lower TC LDL HDLs compared to the general pop). Or... if you eat low fat, low cholesterol, low saturated fatty acids. The interaction is hypothesized to be related to a statin-and/or-fibrate-related apo A1 reduction in activity (and because you are chol/saturated-fatty-acid-deficient).

----> If you'd like to amuse yourself and see how cardio-stat-idiots attempt to debate themselves out of the above clinical findings, read THIS. "We found no significant association of change in HDL cholesterol with the log risk ratio in any model after adjustment for changes in LDL cholesterol." wtf? Note their funding... 'unrestricted grant from... Pfizer.'

Mr. 'LindyBill' (EBT regression 33.6% in one year and 21% HDL increase from 38 to 46 mg/dl with major weight loss of several inches off the abdomen which accounts for 5-7% Body Fat recomposition (eg, utilization of stored 25-30# Sat Fat) via walking/ball-rm-dancing/ swimming daily and low carb diet; stopped simva 20/d a while ago due to aches but no updated labs; READ, NO STATINS)

"Mediterranean diet was not enough for me. As an FH with a TC of 340, I followed the Mediterranean diet approach (high fiber vegan + salmon +sardines) for over 12 years, while I was on 40mg Pravastatin (TC= 220, HDL = 35, LDL = 130), but after severe plantar fasciitis and muscle wasting set in from the Prav. (even on a dosage reduction to 2mg from 40mg), I stopped rx and tested all the other statins and more without success.

The Paleo diet has changed my ability to metabolize fats, reduced my blood glucose levels, and dramatically increased my HDLs (84). On the same daily running and biking regimen, my body fat % dropped from 15.5% to 8% during the last 6 months. I eat huge quantities of non-cereal, non-grain foods all day and continue to lose weight while feeling far more energetic. As an added benefit, at the age of 44, I recently ran a road race at a pace I have not been able to match since I was on the high school track team.I loved to eat legumes and healthy grains, but I have seen such a dramatic improvement that I will never go back."His lipoprotein results with Paleo:"Paleo diet + exercise + psyllium TRIPLED my HDL to 84. I am a slim FH patient who tried and failed to raise my HDL levels above 40 using a low-fat vegetarian, high exercise lifestyle (My LDL was 240). I could not tolerate ANY statin or Welchol. Now, I eat only lean meat, vegetables, fruits and raw nuts while avoiding all sugar, cereals, grains and legumes. With my unchanged intense exercise regimen, I have lost 10 pounds over 6 months, yet grown stronger and faster. I have reduced my LDLs to 202, while raising my HDLs to 84 from as low as 35. At 44, I feel like I have turned the clock back st least a decade. "

Tuesday, June 9, 2009

We've been talking a lot of about increasing dietary saturated fatty acids (SFAs) at TYP. The Part 3 Track Your Plaque Diet was published approximately half a year ago and I've been remiss in not promoting it more sooner.

Pioneering the field of cardiovascular research, regression and plaque tracking, Dr. Davis has been promoting (the below) seven TYP goals for Y E A R S . . . light years ahead of the common conventionalist/ interventionalist. New recent observations made by both researchers investigating atherogenic dyslipidemias and by those conducting long-lived healthy centenarian research are, in fact, aligned with several of these seven TYP goals. Maximixation of plaque control and regression have been observed when these seven goals are optimized (TYP 2.0).

For carotid arteries, achievement of any of the below factors will likely induce entire resolution of atherosclerotic plaque. However for the coronary arteries, regression is slightly tougher for a variety of reasons and achievement of all or nearly all seven will support dramatic coronary calcification regression.

Coronary arteries are thinner and more affected by systemic inflammation and the shearing forces secondary to high blood pressure (whether during physical exertion or at rest).

On the other hand, for stabilization and completeeliminationof coronary events (angioplasty, stent, MI, bypass or death), gaining control of only three out seven is right on the money... imo.

We define stabilization as EBT CAC score progression of less than 10-20% annual increase.

The average American increase is 30-60% annually (of course faster in Lp(a), apo E4, diabetes and MetSyn).

Wouldn't you like your investment portfolio to grow as fast as American plaque?

6) Sufficient omega-3 ALA and EPA DHA (fatty acid profile, AA:EPA ratio of 1.5-2.0:1; if we flip the ratio around to EPA:AA, in other words omega-3 to omega-6 ratio of 1:1.5, then we're talking 60% of our RBC/cellular membranes being enriched with omega-3 PUFAs content versus omega-6 PUFAs. We really like 60% for some reason at TYP...go figure.)

(LDL = 60 mg/dl is #8 and IMO optional -- this is the easiest with synthetic drugs but unfortunately it prevents #1-4 for some low chol/low fat folks)

VLCD + Cholesterol + SFAs Support 'Super-TYP' Goals #1 through 4

Dr.Volek has published numerous articles on nutrition and metabolism in regards to the benefits of VLCD (very low carb diets) and ketogenic diets in controlling insulin and other hormones. He has shown in various studies how very low carb diets shift small dense LDL particles (atherogenic) to large, fluffy, buoyant LDL particles (regressive). Cholesterol and SFAs (saturated fatty acids) from eggs were demonstrated by Volek to be particularly effective at promoting larger HDL particles, the 'good' cholesterol associated with plaque regression, longevity and cancer protection.

Long-lived centenarians, also known as probands, had lipoprotein analyses performed via NMR. Of the markers tracked, four out of seven TYP goals were achieved. Interestingly, centenarian data shows that they still display vitamin D deficiency like the rest of us.

See picture (top)

Figure 2 displaying the Percentage of Large and Small HDL and LDL Particle Sizes in Long-Lived Probands, Offspring, and Ashkenazi and Framingham Controls HDL indicates high-density lipoprotein; LDL, low-density lipoprotein. *P less than .001 for probands vs Ashkenazi and Framingham controls and P less than .001 for offspring vs Ashkenazi and Framingham controls for both large and small HDL and LDL particle sizes.

1) Small-Dense-LDL =< 10% of total LDL particles (irregardless of total LDL on NMR or VAP) (TYP Goal)

Apparently this sub-population of Ashkenazi Jewish have a genotype variation on the CETP gene which regulates and controls HDL-particle sizes. HDL-cholesterol is an antioxidant and they have the genetic ability to upregulate Large-HDL particles more than the rest of us. Their offspring may have version as well. The offspring (and controls, who were the spouse of the offspring) who were free of any chronic conditions (no hypertension, no metabolic syndrome, no cardiovascular disease) incidentally displayed similar high HDL particle counts, large HDL and LDL particle sizing and buoyancy, and reached the TYP goals of greater 60% Large-LDL and greater than 50% Large-HDL. Their counterparts with chronic conditions failed to meet these goals.

Volek et al have demonstrated how one can achieve control of small dense LDL via inhibition of CETP activity by a very low carb diet/HIGH-FAT DIET with additions of dietary eggs/cholesterol/SFAs.

Can we obtain similar sd-LDL less than of 10% lipoprotein profiles as long-lived heart-disease-free, cancer-free centenarians? We may not have the genetic programming/genotype but I certainly believe with our current understanding and technology, achievement of the centenarian phenotype is a definable undertaking.

The low-fat diet contained 24% of energy as fat (6% saturated, 12% monounsaturated, and 4% polyunsaturated) and 59% as carbohydrate, with equal amounts of simple and complexcarbohydrates and 17% as protein.

The high-fat diet contained 46% of energy as fat (18% saturated, 13% monounsaturated, and 12% polyunsaturated) and 39% as carbohydrate and 15% as protein.

STUDY DESIGN: They tested whether nutrient intakes estimated from 4-d diet records were associated with plasma lipoprotein subclasses in 103 men who were randomly assigned to a low-fat (24% fat) and a high-fat (46% fat) diet for 6 wk each in a crossover design. Carbohydrates (~20% of energy) were basically substituted out for dietary fat intake.

An increase in saturated fat, and in particular, myristic acid, was associated with increases in larger LDL particles (and decreases in smaller LDL particles).

Studies of the relation between LDL subclasses and CAD have, in contrast, established that a predominance of small, dense LDL particles (LDL subclass pattern B) is associated with increased risk of myocardial infarction (47, 48) and angiographically documented CAD (48–50). Some studies have also shown that small LDL particles are potentially more atherogenic than larger LDL because of increased susceptibility to oxidation (51, 52) and increased promotion of intracellular cholesterol ester accumulation (53). In addition, reductions in small LDL particles, not in larger LDL particles, have been associated with decreased CAD progression (54, 55).

So the authors do discuss the value of reducing sd-LDL, the holy grail of heart disease sufferers. The discussion on the benefits of a saturated fat intake of 18% however seemed to be quite curt and short though.

In fact, I couldn't even find it.

What we know about lipoproteins at TYP is that the bigger, the better. And the statements made by Krauss definitely confirms our current understanding.

The profound enlargement of Large-LDL (I and II) and HDL-2 in healthy men is quite extraordinary ad remarkable in only 6 weeks. No drugs involved, diet alone. In one the next few posts, we'll examine a heart disease population, including post-CABG men and women, and the benefits, again, of a high saturated fat diet.

For vegetarian sources, virgin coconut oil is a good sub, containing shorter SFAs (medium-chain) lauric and caprylic acid. Sat Fat 18% of a 2000 Kcal/d diet would be equivalent to 40 grams of coconut oil (fat is 9 kcal/g).

Or 2.8 Tablespoons VCO daily.

My HDLs Increased 18.0% With Coconut Oil
Like many Paleo fans, I have observed an increase in my HDLs from 89 mg/dl back in 12/2008 to now 105 mg/dl. It's now almost ~12 mos gluten free, baby. Wow. What a year.

About 6-8 wks prior to the blood test, we started cooking with VCO, virgin coconut oil (+smearing it all over my body after showers...no studies to back justification *haa* but it's nice cheap and works, eg less wrinkles, better healing, maybe better HDLs).

TGs came down from 80s to now 60s mg/dl.

Both the LDL is now higher 120s mg/dl (directly measured, not Friedewald) and TC in the 240s like some long-living healthy female elderly and centenarians.